We propose to further define the factors controlling arterial PO2 in acute atelectasis and pulmonary edema. To do so, we will study mechanisms regulating pulmonary blood flow to acutely atelectatic, edematous and hypoxia lobes of the lung. Hypoxic pulmonary vasoconstriction normally directs flow away from these areas, but this effect may be antagonized by unknown factors. We have shown that the pulsatility of pulmonary blood flow, and that systemic hypoxemia are two such antagonizing factors. We hypothesize that these factors may be related, since distensibility of large pulmonary arteries is reduced in systemic hypoxemi and reducing arterial distensibility may increase the pulsatility of pulmonary blood flow. Increased pulmonary arterial pressure with increasing pulmonary blood flow may also antagonize hypoxic vasoconstriction by reducing distensibility of the pulmonary arterial walls as they approach their elastic limit. The altered compliance of the pulmonary parenchyma in pulmonary edema may also antagonize hypoxic vasoconstriction by a similar interaction, reducing the ability of large pulmonary vessels to store blood during systole. We will bypass the right ventricle of dogs with a piston type pump and measure total blood flow by electromagnetic flowmeters during left lung collapse over a wide range of total flows. A damper will then be added after the pump, and the study repeated at identical mean pressures but with steady flow. If an elastic limit of the pulmonary vessels is reached at the higher mean pressures, then diversion of pulsatile flow should be equally well diverted from the collapsed lung. We will also induce oleic acid edema in the left lung of dogs, and measure the blood flow to that lung during artificial ventilation with different levels of positive end-expiratory pressure. These responses will be compared with those seen in atelectatic lung, and those seen in a diffuse oleic acid-induced edema in both lungs. The partition of blood flow between hypoxic atelectatic or endemous lungs and normal lungs will also be studied as cardiac output is increased in the intact animal by opening peripheral arterio-venous fistulae.